Bedsores, technically known as pressure ulcers or decubitus, are lesions caused by unrelieved pressure to any part of the body, especially over bony or cartilaginous areas. These sores are generally completely treatable if detected early, but without medical attention they can be fatal. Pressure sores can trigger other ailments, causing considerable suffering and financial cost. Brem, H., Kirsner, R. S., and Falanga, V., “Protocol for the successful treatment of venous ulcers,” Am. J Surgery, 188(1 Supp. 1):1-8 (July 2004). Potential complications include autonomic dysreflexia, bladder distension, osteomyelitis, pyarthroses, sepsis, amyloidosis, anemia, urethral fistula, gangrene and very rarely malignant transformation. Sores often recur because patients do not follow recommended treatment or develop seromas, hematomas, infections, or dehiscence. Paralytic patients are the most likely people to have pressure sores recur. In some cases, complications from pressure sores can be life-threatening. The most common causes of fatality stem from renal failure and amyloidosis. As currently defined by the U.S. National Pressure Ulcer Advisory Panel (NPUAP), pressure ulcers have four recognized stages, as follows:
STAGE I: superficial, accompanied by redness that does not subside after pressure is relieved. This stage is visually similar to reactive hyperemia (i.e., excessive redness) in skin after prolonged application of pressure. Stage I pressure ulcers are distinguished from reactive hyperemia because: a) reactive hyperemia resolves itself within three quarters of the time over which pressure was applied, and b) reactive hyperemia blanches when pressure is applied, whereas a Stage I pressure ulcer does not. Stage 1 pressure ulcer skin may be hotter or cooler than normal, have an odd texture, or perhaps be painful to the patient. Whereas there is obvious redness on light-skinned patients, ulcers on darker-skinned individuals may be shades of purple or blue in comparison to lighter skin tones.
STAGE II: includes damage to the epidermis extending into but no deeper than the dermis. A stage 2 ulcer may be termed a blister or abrasion.
STAGE III: involves the full thickness of skin and may extend into subcutaneous tissue. The blood supply is relatively poor and can be difficult to heal. There may also be subsurface damage that is more extensive than appears on the surface.
STAGE IV: extends into the muscle, tendon or even bone.
UNSTAGEABLE pressure ulcers are those covered with dead cells (i.e., eschar) and exudate from the wound, such that the pressure ulcer depth cannot be determined.
Higher stage wounds require prolonged healing times. About 75% of Stage II ulcers heal within eight weeks. For Stage IV pressure ulcers only 62% ever heal, and only 52% heal within one year. Thomas, D. R., Diebold, M. R., Eggemeyer, L. M., “A controlled, randomized, comparative study of a radiant heat bandage on the healing of stage 3-4 pressure ulcers: A pilot study.” J. Am. Med. Dir. Assoc., 6(1):46-49 (January-February 2005). Counterintuitively, pressure ulcers do not regress in stage as they heal. A pressure ulcer that becomes shallower with healing is described in terms of its original deepest depth (e.g., a healing Stage II pressure ulcer).
Three forces account for bedsore etiology. First, Tissue compression arises from the force of bone against a surface, as when a patient remains in a single decubitus position for a lengthy period. This results in decreased tissue perfusion; ischemia occurs and can lead to tissue necrosis if left untreated in an immunocompromised patient. Second, shear forces arising in prolonged single decubitus positions result when the deep fascia and skeletal muscle slides down under the force of gravity, thus blood vessels can be pinched off and ischemia and tissue necrosis may occur. Finally, friction forces resist the shearing of skin, and thus can cause excess shedding of epidermal layers. The etiology may be aggravated by other conditions. Excess moisture from incontinence, perspiration or exudate may weaken adhesion between epithelial cells and thereby cause maceration of the epidermis. Age, malnutrition, vascular disease, diabetes mellitus and smoking are some other factors that can affect the etiology. The exact mechanism of etiology is not completely clear: it may be due to the injury of deep tissue that spreads outward to the epidermis, or possibly it may be due to a top-down deterioration that begins at the surface of the skin. Niezgoda, J. A., Mendez-Eastman, S. “The effective management of pressure ulcers,” Advances in Skin & Wound Care: The Journal for Prevention and Healing, 19(1-Supp.):3-15 (2006).
The incidence of bedsores varies widely and depends in part on the type of care. For acute care, the range is 0.4% to 38% incidence. For long-term care it is 2.2% to 23.9%. For home care it is 0% to 29%. Intensive care units have higher rates (8% to 40%) because their patients are more often immunocompromised. NPUAP Board of Directors, “Pressure ulcers in America: prevalence, incidence, and implications for the future,” in An Executive Summary of the NPUAP Monograph, ed. Cuddigan, J., et al., (July/August 2001), The risk of developing bedsores can be determined by using the Braden Scale for Predicting Ulcer Pressure Risk, using six categories: sensory perception; moisture; activity; mobility; nutrition; and friction and shear. The best possible score is 23; the worst is 6. For a total score below 11 the patient is at risk of developing bedsores. Jiricka, M K, Ryan, P, Carvalho, M A, and Bukvich, J, “Pressure ulcer risk factors in an ICU population,” Am. J. Crit. Care, 4(5):361-367 (1995).
To date the effective healing of bedsores has typically required a multidisciplinary approach and teamwork among specialists along six lines of treatment. (see, e.g., Rothrock, J. C., Alexander's Care of the Patient in Surgery, 13th ed. (Mosby, 2007).
1. Debridement—necrotic tissue must be removed during treatment in order to minimize bacterial growth. Several methods are currently in use for debridement. Niezgoda, J. A., Mendez-Eastman, S., “The Effective Management of Pressure Ulcers.” Advances in Skin & Wound Care: The Journal for Prevention and Healing, 19(1—Supp.): 3-15 (2006). These methods vary in effectiveness and speed, and some are painful. They include: the use of moist dressings to aid the body's own digestion enzymes (autolytic debridement); the use of medical maggots (biological debridement, see http://www.fda.gov/cdrh/510k/sumjan04.html); tearing off dressings that are applied wet and removed when dry (mechanical debridement); scraping necrotic tissue off with a scalpel (sharp debridement); surgical removal (surgical debridement); and separation of necrotic and healthy tissue sonically (ultrasound-assisted wound therapy).
2. Infection control—to avoid breeding bacteria in purulent discharge, particularly in immunocompromised patients. Additional symptoms of systemic infection include fever, pain, erythema, oedema, and warmth of the area; infected wounds may also have a gangrenous smell, be discoloured, and eventually exude even more pus. Antiseptics and antimicrobials are typically applied immediately; experts advise against the use of hydrogen peroxide for this purpose due to its potential toxicity to the wound. Recently introduced wound dressings for this purpose have cadexomer iodine and silver in them. Duoderm is often used on smaller wounds to both provide comfort and protect them from outside air and infections. Systemic antibiotics are typically avoided when treating infection of a bedsore, because it can lead to bacterial resistance.
3. Diet—dietitians are often consulted to ensure that the patient ingests enough protein to ensure tissue repair. Lab tests for serum albumin and lymphocyte counts as well as bioelectrical impedance analysis are typical diagnostic tools. Nutritional supplementation may include but is not limited to, arginine, glutamine, vitamin A, vitamin B complex, vitamin E, vitamin C, magnesium, manganese, selenium and zinc, all under a physician's care to prevent the use of detrimental incorrect dosages.
4. Pressure relief—once a bedsore is found, pressure on it must be removed immediately and the patient turned at least once every two hours to avoid aggravating the wound. Nursing homes and hospitals usually have bedsore prevention programs employing a standing frame to reduce pressure, and ensure dry sheets by means of catheters or impermeable dressings. For paralyzed individuals, a pressure shifting schedule and pressure relief cushions can be effective. Pressure distributive mattresses can also be used. Methods to evaluate efficacy of these products were only recently developed. Bain, D. S., Ferguson-Pell, M. W., “Remote monitoring of sitting behaviour of people with spinal injury,” J. Rehab. Res. Dev., 39(4):513-520 (July 2002).
5. Caregiver education—especially for home-based care, a family must be educated about how to treat their loved one's pressure ulcers. The training includes among things the proper way to turn a patient, how to properly dress the wound, proper nutrition for the patient, and how to deal with crisis. Because of the difficulty psychological consultants for the home caregiver are sometimes recommended.
6. Wound intervention—this depends on the stage of the bedsore. Stage I and II ulcers are treated under the guidelines of the American Medical Directors Association (AMDA). Stage III and IV ulcers often receive surgery such as closure methods (e.g., tissue flap, skin graft) or topical negative pressure wound therapy by means of a foam that is held the wound cavity by a film with an airtight seal. Progress under negative pressure therapy is reevaluated every two weeks. Negative pressure therapy is contraindicated for patients who have not been prepared or had previous steps toward recovery, or where the wound has in inadequate circulation, is raw and debrided, has necrotized tissue and eschar, or is fibrotic. Topical ointments such as the zinc oxide-based Sensicure™ are also sometimes used, as are alcohol wipes, but these have not proved to be particularly effective in accelerating healing.
As is clear from the description above, the incidence of bedsores is widespread, these sores represent a great hazard to health, and not only have they healed very slowly at best, but they are both difficult and expensive to treat. There is, then, an ongoing need for therapies to prevent and treat bedsores in a rapid, thrifty and efficacious manner. Several types of cuts and burns present comparable challenges for clinical medicine, and there is an ongoing need for a treatment method that can accelerate their healing as well.